Guidance for the Distribution of Pulse Oximeters to Patients at Increased Risk for Severe COVID-19
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Approach to Cyanosis in a Neonate.Pdf
PedsCases Podcast Scripts This podcast can be accessed at www.pedscases.com, Apple Podcasting, Spotify, or your favourite podcasting app. Approach to Cyanosis in a Neonate Developed by Michelle Fric and Dr. Georgeta Apostol for PedsCases.com. June 29, 2020 Introduction Hello, and welcome to this pedscases podcast on an approach to cyanosis in a neonate. My name is Michelle Fric and I am a fourth-year medical student at the University of Alberta. This podcast was made in collaboration with Dr. Georgeta Apostol, a general pediatrician at the Royal Alexandra Hospital Pediatrics Clinic in Edmonton, Alberta. Cyanosis refers to a bluish discoloration of the skin or mucous membranes and is a common finding in newborns. It is a clinical manifestation of the desaturation of arterial or capillary blood and may indicate serious hemodynamic instability. It is important to have an approach to cyanosis, as it can be your only sign of a life-threatening illness. The goal of this podcast is to develop this approach to a cyanotic newborn with a focus on these can’t miss diagnoses. After listening to this podcast, the learner should be able to: 1. Define cyanosis 2. Assess and recognize a cyanotic infant 3. Develop a differential diagnosis 4. Identify immediate investigations and management for a cyanotic infant Background Cyanosis can be further broken down into peripheral and central cyanosis. It is important to distinguish these as it can help you to formulate a differential diagnosis and identify cases that are life-threatening. Peripheral cyanosis affects the distal extremities resulting in blue color of the hands and feet, while the rest of the body remains pinkish and well perfused. -
Practical Cardiac Auscultation
LWW/CCNQ LWWJ306-08 March 7, 2007 23:32 Char Count= Crit Care Nurs Q Vol. 30, No. 2, pp. 166–180 Copyright c 2007 Wolters Kluwer Health | Lippincott Williams & Wilkins Practical Cardiac Auscultation Daniel M. Shindler, MD, FACC This article focuses on the practical use of the stethoscope. The art of the cardiac physical exam- ination includes skillful auscultation. The article provides the author’s personal approach to the patient for the purpose of best hearing, recognizing, and interpreting heart sounds and murmurs. It should be used as a brief introduction to the art of auscultation. This article also attempts to illustrate heart sounds and murmurs by using words and letters to phonate the sounds, and by presenting practical clinical examples where auscultation clearly influences cardiac diagnosis and treatment. The clinical sections attempt to go beyond what is available in standard textbooks by providing information and stethoscope techniques that are valuable and useful at the bedside. Key words: auscultation, murmur, stethoscope HIS article focuses on the practical use mastered at the bedside. This article also at- T of the stethoscope. The art of the cardiac tempts to illustrate heart sounds and mur- physical examination includes skillful auscul- murs by using words and letters to phonate tation. Even in an era of advanced easily avail- the sounds, and by presenting practical clin- able technological bedside diagnostic tech- ical examples where auscultation clearly in- niques such as echocardiography, there is still fluences cardiac diagnosis and treatment. We an important role for the hands-on approach begin by discussing proper stethoscope selec- to the patient for the purpose of evaluat- tion and use. -
Asphyxia Neonatorum
CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well being develop as a result of perinatal asphyxia. Central nervous system ab normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in molecules brought into the alveoli inadequately com Pjury in the newborn. Severe birth asphyxia, evi pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul deprivation has been further enriched by investigators monary capillary blood. -
Mosby: Mosby's Nursing Video Skills
Mosby: Mosby's Nursing Video Skills Procedural Guideline for Assessing Apical Pulse Procedure Steps 1. Verify the health care provider’s orders. 2. Gather the necessary equipment and supplies. 3. Perform hand hygiene. 4. Provide for the patient’s privacy. 5. Introduce yourself to the patient and family if present. 6. Identify the patient using two identifiers. 7. Assess for factors that can affect the apical pulse rate and rhythm, such as medical history, disease processes, age, exercise, position changes, medications, temperature, or sympathetic stimulation. 8. Gloves are only worn if nurse will be in contact with bodily fluids or the patient is in protective precautions. 9. Help the patient into a supine or sitting position, and expose the sternum and the left side of the chest. 10. Locate the point of maximal impulse (PMI, or apical impulse). To do this, find the angle of Louis, which feels like a bony prominence just below the suprasternal notch. 11. Slide your fingers down each side of the angle to find the second intercostal space (ICS). Carefully move your fingers down the left side of the sternum to the fifth intercostal space and over to the left midclavicular line. 12. Feel the PMI as a light tap about 1 to 2 centimeters in diameter, reflecting the apex of the heart. 13. If the PMI is not where you would expect, as in a patient whose left ventricle is enlarged, inch your fingers along the fifth intercostal space until you feel the PMI. 14. Remember where you felt the PMI: over the apex of the heart in the fifth intercostal space at the left midclavicular line. -
Clinical Management of Severe Acute Respiratory Infections When Novel Coronavirus Is Suspected: What to Do and What Not to Do
INTERIM GUIDANCE DOCUMENT Clinical management of severe acute respiratory infections when novel coronavirus is suspected: What to do and what not to do Introduction 2 Section 1. Early recognition and management 3 Section 2. Management of severe respiratory distress, hypoxemia and ARDS 6 Section 3. Management of septic shock 8 Section 4. Prevention of complications 9 References 10 Acknowledgements 12 Introduction The emergence of novel coronavirus in 2012 (see http://www.who.int/csr/disease/coronavirus_infections/en/index. html for the latest updates) has presented challenges for clinical management. Pneumonia has been the most common clinical presentation; five patients developed Acute Respira- tory Distress Syndrome (ARDS). Renal failure, pericarditis and disseminated intravascular coagulation (DIC) have also occurred. Our knowledge of the clinical features of coronavirus infection is limited and no virus-specific preven- tion or treatment (e.g. vaccine or antiviral drugs) is available. Thus, this interim guidance document aims to help clinicians with supportive management of patients who have acute respiratory failure and septic shock as a consequence of severe infection. Because other complications have been seen (renal failure, pericarditis, DIC, as above) clinicians should monitor for the development of these and other complications of severe infection and treat them according to local management guidelines. As all confirmed cases reported to date have occurred in adults, this document focuses on the care of adolescents and adults. Paediatric considerations will be added later. This document will be updated as more information becomes available and after the revised Surviving Sepsis Campaign Guidelines are published later this year (1). This document is for clinicians taking care of critically ill patients with severe acute respiratory infec- tion (SARI). -
Respiratory and Gastrointestinal Involvement in Birth Asphyxia
Academic Journal of Pediatrics & Neonatology ISSN 2474-7521 Research Article Acad J Ped Neonatol Volume 6 Issue 4 - May 2018 Copyright © All rights are reserved by Dr Rohit Vohra DOI: 10.19080/AJPN.2018.06.555751 Respiratory and Gastrointestinal Involvement in Birth Asphyxia Rohit Vohra1*, Vivek Singh2, Minakshi Bansal3 and Divyank Pathak4 1Senior resident, Sir Ganga Ram Hospital, India 2Junior Resident, Pravara Institute of Medical Sciences, India 3Fellow pediatrichematology, Sir Ganga Ram Hospital, India 4Resident, Pravara Institute of Medical Sciences, India Submission: December 01, 2017; Published: May 14, 2018 *Corresponding author: Dr Rohit Vohra, Senior resident, Sir Ganga Ram Hospital, 22/2A Tilaknagar, New Delhi-110018, India, Tel: 9717995787; Email: Abstract Background: The healthy fetus or newborn is equipped with a range of adaptive, strategies to reduce overall oxygen consumption and protect vital organs such as the heart and brain during asphyxia. Acute injury occurs when the severity of asphyxia exceeds the capacity of the system to maintain cellular metabolism within vulnerable regions. Impairment in oxygen delivery damage all organ system including pulmonary and gastrointestinal tract. The pulmonary effects of asphyxia include increased pulmonary vascular resistance, pulmonary hemorrhage, pulmonary edema secondary to cardiac failure, and possibly failure of surfactant production with secondary hyaline membrane disease (acute respiratory distress syndrome).Gastrointestinal damage might include injury to the bowel wall, which can be mucosal or full thickness and even involve perforation Material and methods: This is a prospective observational hospital based study carried out on 152 asphyxiated neonates admitted in NICU of Rural Medical College of Pravara Institute of Medical Sciences, Loni, Ahmednagar, Maharashtra from September 2013 to August 2015. -
Chronic Hypoxemia in the Newborn Lamb: Cardiovascular, Hematopoietic, and Growth Adaptations
003 1-3998/85/19 10-l004$02.00/0 PEDIATRIC RESEARCH Val. 19, No. 10, 1985 Copyright O 1985 International Pediatric Research Foundation, Inc. Printed in U.S. A. Chronic Hypoxemia in the Newborn Lamb: Cardiovascular, Hematopoietic, and Growth Adaptations DAVID TEITEL, DANIEL SIDI,' DANIEL BERNSTEIN, MICHAEL A. HEYMANN, AND ABRAHAM M. RUDOLPH Cardiovascular Research Institute and the Departments of Pediatrics, Physiology, and Obstetrics, Gynecology and Reproductive Sciences, University of California, Sun Francisco, California 94143 ABSTRAm. We have created a model of chronic hypox- developed a model of a common cyanotic heart lesion to assess emia in the newborn lamb by decreasing pulmonary blood some of its cardiovascular and metabolic effects on the newborn flow in the presence of an atrial septal defect. Via a left lamb. lateral thoracotomy, we place an inflatable balloon around Several authors have studied acute hypoxemia in the devel- the pulmonary artery and perform an atrial septostomy oping organism and elucidated its effects on general cardiovas- under direct vision. We also insert several vascular cathe- cular function (1-3), regional blood flow (1, 4, 5), metabolic ters and place an electromagnetic flow transducer around activity (6, 7), and course of decompensation (1). The effects of the ascending aorta. Three days after surgery, we inflated sympathetic blockade (8, 9) and decreasing Hb oxygen affinity the balloon in 11 lambs such that arterial oxygen saturation (10, 11) on the response to acute hypoxemia have also been decreased to 60 to 75%. Studies were performed on these addressed. Few studies have been performed on the chronically lambs twice weekly and weekly on 12 normoxemic lambs. -
Bradycardia; Pulse Present
Bradycardia; Pulse Present History Signs and Symptoms Differential • Past medical history • HR < 60/min with hypotension, acute • Acute myocardial infarction • Medications altered mental status, chest pain, • Hypoxia / Hypothermia • Beta-Blockers acute CHF, seizures, syncope, or • Pacemaker failure • Calcium channel blockers shock secondary to bradycardia • Sinus bradycardia • Clonidine • Chest pain • Head injury (elevated ICP) or Stroke • Digoxin • Respiratory distress • Spinal cord lesion • Pacemaker • Hypotension or Shock • Sick sinus syndrome • Altered mental status • AV blocks (1°, 2°, or 3°) • Syncope • Overdose Heart Rate < 60 / min and Symptomatic: Exit to Hypotension, Acute AMS, Ischemic Chest Pain, Appropriate NO Acute CHF, Seizures, Syncope, or Shock Protocol(s) secondary to bradycardia Typically HR < 50 / min YES Airway Protocol(s) AR 1, 2, 3 if indicated Respiratory Distress Reversible Causes Protocol AR 4 if indicated Hypovolemia Hypoxia Chest Pain: Cardiac and STEMI Section Cardiac Protocol Adult Protocol AC 4 Hydrogen ion (acidosis) if indicated Hypothermia Hypo / Hyperkalemia Search for Reversible Causes B Tension pneumothorax 12 Lead ECG Procedure Tamponade; cardiac Toxins Suspected Beta- IV / IO Protocol UP 6 Thrombosis; pulmonary Blocker or Calcium P Cardiac Monitor (PE) Channel Blocker Thrombosis; coronary (MI) A Follow Overdose/ Toxic Ingestion Protocol TE 7 P If No Improvement Transcutaneous Pacing Procedure P (Consider earlier in 2nd or 3rd AVB) Notify Destination or Contact Medical Control Revised AC 2 01/01/2021 Any local EMS System changes to this document must follow the NC OEMS Protocol Change Policy and be approved by OEMS 1 Bradycardia; Pulse Present Adult Cardiac Adult Section Protocol Pearls • Recommended Exam: Mental Status, HEENT, Skin, Heart, Lungs, Abdomen, Back, Extremities, Neuro • Identifying signs and symptoms of poor perfusion caused by bradycardia are paramount. -
Arrhythmia What Is It?
Arrhythmia What is it? Most of us have felt our heart race or skip a beat. It’s fairly normal every once and a while. But for some people, it’s a sign of arrhythmia – a disorder of your heart rate or rhythm – that needs to be checked out by a specialist. If you have an arrhythmia (there are multiple types), your heart either beats: • too fast • too slow or • with an irregular pattern Did You Know? This change in your heart rhythm is usually caused by a “glitch” Our heart beats an average of in your heart’s electrical activity, which tells the heart when to 70 to 80 times a minute and contract and pump blood to the body. Your heart doesn’t beat over 100,000 times a day! It’s with the regularity of a Swiss watch, and many factors can cause no wonder millions of people an irregularity. notice palpitations such as skipping a beat, fluttering or a Some of these factors include: racing heart. • having had a heart attack • having heart failure • blood chemistry imbalances • abnormal hormone levels • alcohol, caffeine and other substances or medicines • a variety of inherited abnormalities 8 Tips for Staying Heart Healthy with Arrhythmias Living with an arrhythmia varies tremendously from one person to the next. It will depend on the type of arrhythmia you have, how serious it is and the recommended treatment. Some people can take a single medication to correct their heart’s rhythm; others undergo electrophysiology studies or require a pacemaker or implantable defibrillator. No matter what kind of arrhythmia you have, there are things you can do to keep your heart healthy and ticking as it should. -
5 Precordial Pulsations
Chapter 5 / Precordial Pulsations 113 5 Precordial Pulsations CONTENTS MECHANICS AND PHYSIOLOGY OF THE NORMAL APICAL IMPULSE PHYSICAL PRINCIPLES GOVERNING THE FORMATION OF THE APICAL IMPULSE NORMAL APICAL IMPULSE AND ITS DETERMINANTS ASSESSMENT OF THE APICAL IMPULSE LEFT PARASTERNAL AND STERNAL MOVEMENTS RIGHT PARASTERNAL MOVEMENT PULSATIONS OVER THE CLAVICULAR HEADS PULSATIONS OVER THE SECOND AND/OR THIRD LEFT INTERCOSTAL SPACES SUBXIPHOID IMPULSE PRACTICAL POINTS IN THE CLINICAL ASSESSMENT OF PRECORDIAL PULSATIONS REFERENCES In this chapter the pulsations of the precordium will be discussed in relation to their identification, the mechanisms of their origin, and their pathophysiological and clinical significance. Precordial pulsations include the “apical impulse,” left parasternal movement, right parasternal movement, pulsations of the clavicular heads, pulsations over the second left intercostal space, and subxiphoid impulses. MECHANICS AND PHYSIOLOGY OF THE NORMAL APICAL IMPULSE Since during systole the heart contracts, becoming smaller and therefore moving away from the chest wall, why should one feel a systolic outward movement (the apical impulse) at all? Logically speaking there should not be an apical impulse. Several different methods of recording the precordial motion have been used to study the apical impulse going back to the late 19th century (1,2). Among the more modern methods, the notable ones are the recordings of the apexcardiogram (3–17), the impulse cardiogram (18), and the kinetocardiogram (19–21). While apexcardiography records the relative displacement of the chest wall under the transducer pickup device, which is often held by the examiner’s hands, the proponents of the impulse cardiography and kinetocardiography point out that these methods allow the recording of the absolute movement of the chest wall because the pickup device is anchored to a fixed point held 113 114 Cardiac Physical Examination in space away from the chest. -
Pathophysiology and Treatment of Cheyne-Stokes Respiration Thorax: First Published As 10.1136/Thx.53.6.514 on 1 June 1998
514 Thorax 1998;53:514–518 Pathophysiology and treatment of Cheyne-Stokes respiration Thorax: first published as 10.1136/thx.53.6.514 on 1 June 1998. Downloaded from M T Naughton Cheyne-Stokes respiration is a disorder charac- results from hyperventilation, prolonged circu- terised by recurrent central apnoeas during lation time, and reduced blood gas buVering sleep alternating with a crescendo-decrescendo capacity.21 pattern of tidal volume.12 It is often observed in patients with congestive heart failure, usually HYPERVENTILATION during stages 1 and 2 non-REM sleep when Hyperventilation, the common pathophysi- ventilation is under chemical-metabolic ological feature of all forms of periodic breath- 2 control. Patients with Cheyne-Stokes respira- ing, causes PaCO2 levels to fall below the tion usually present with the symptoms of apnoeic threshold triggering a central apnoea. orthopnoea, paroxysmal nocturnal dyspnoea, Once the peripheral chemoreceptors sense an excessive daytime sleepiness and witnessed apnoea related rise in the PaCO2 level above the apnoeas in the setting of congestive heart apnoea threshold, hyperventilation recurs driv- 13 failure. Excessive weight and snoring may be ing the PaCO2 level below the apnoea threshold absent. Approximately 50% of patients with once again.2 symptomatic congestive heart failure have Increased central hypercapnic ventilatory sleep apnoea, mainly of the Cheyne-Stokes responsiveness has been reported to occur in respiration variety.4-6 As congestive heart failure Cheyne-Stokes respiration with congestive occurs in 1% of the adult population and dou- heart failure22 and in other forms of periodic bles in prevalence for each decade beyond 60 breathing in subjects without congestive heart years,7 Cheyne-Stokes respiration is common failure—namely, idiopathic non-hypercapnic but often left unrecognised. -
Jugular Venous Pressure
NURSING Jugular Venous Pressure: Measuring PRACTICE & SKILL What is Measuring Jugular Venous Pressure? Measuring jugular venous pressure (JVP) is a noninvasive physical examination technique used to indirectly measure central venous pressure(i.e., the pressure of the blood in the superior and inferior vena cava close to the right atrium). It is a part of a complete cardiovascular assessment. (For more information on cardiovascular assessment in adults, see Nursing Practice & Skill ... Physical Assessment: Performing a Cardiovascular Assessment in Adults ) › What: Measuring JVP is a screening mechanism to identify abnormalities in venous return, blood volume, and right heart hemodynamics › How: JVP is determined by measuring the vertical distance between the sternal angle and the highest point of the visible venous pulsation in the internal jugular vein orthe height of the column of blood in the external jugular vein › Where: JVP can be measured in inpatient, outpatient, and residential settings › Who: Nurses, nurse practitioners, physician assistants, and treating clinicians can measure JVP as part of a complete cardiovascular assessment What is the Desired Outcome of Measuring Jugular Venous Pressure? › The desired outcome of measuring JVP is to establish the patient’s JVP within the normal range or for abnormal JVP to be identified so that appropriate treatment may be initiated. Patients’ level of activity should not be affected by having had the JVP measured ICD-9 Why is Measuring Jugular Venous Pressure Important? 89.62 › The JVP is